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General Medicine & Family Medicine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the mechanism for type I diabetes mellitus (DM)?

A

Insulin deficiency

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2
Q

What is the mechanism for type II DM?

A

Insulin resistance

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3
Q

What are the main differences between type I and II DM in terms of age of onset, autoimmunity, body habitus, and risk for ketosis?

A
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4
Q

Which autoantibodies can be positive in type I DM?

A
  • Anti-islet cell
  • antiglutamic acid dehydrogenase antibodies
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5
Q

Does the absence of autoantibodies rule out the diagnosis of type I DM?

A
  • No.
  • Some patients with type I DM do not have autoantibodies, and
  • some with type II DM do.
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6
Q

What are some classic presenting symptoms of DM?

A
  • Polyuria
  • polydipsia
  • unexplained weight loss
  • blurry vision
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7
Q

How do you diagnose diabetes?

A
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8
Q

What do you do after an abnormal test?

A
  • Confirm the diagnosis on a subsequent day by using FBG, OGTT, or HbA1c. Patients with glucose ≥200 mg/dL and classic symptoms do not need repeat testing.
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9
Q

What is prediabetes?

A
  • Impaired fasting glucose and/or impaired glucose tolerance
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10
Q

What is the clinical implications of prediabetes ?

A
  • Patients with prediabetes have an increased risk for future development of diabetes mellitus and macrovascular disease.
  • They have a 50% increased risk for myocardial infarction or stroke.
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11
Q

What behavior changes should you encourage in a patient with prediabetes?

A
  • Smoking cessation
  • weight loss (5%-10%)
  • diet changes
  • exercise (30 minutes per day, five times per week)
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12
Q

Why is it important to identify patients with prediabetes?

A
  • Lifestyle modifications can delay and even prevent progression to diabetes.
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13
Q

What are the three main microvascular complicaitons of diabetes?

A
  1. Retinopathy
  2. Nephropathy
  3. Neuropathy
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14
Q

What are the three main macrovascular complications of diabetes?

A
  1. Atherosclerosis
  2. Cerebrovascular disease
  3. Peripheral vascular disease
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15
Q

How frequently should diabetics be seen by an ophthalmologist?

A
  • annually
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16
Q

What is the incidence of retinopathy in patients who have had type II DM for 20 years?

A

50%-80%

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17
Q

What is usually the first sign of diabetic kidney damage?

A

Microalbuminuria

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18
Q

What medication can help reduce the risk of diabetic nephropathy?

A

Angiotensin-converting enzyme inhibitors or angiotension II receptor blockers

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19
Q

What are the different types of diabetic neuropathies?

A
  • Peripheral, autonomic, mononeuropathy (eg, cranial nerve palsy)
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20
Q

Describe the manifestations of diabetic peripheral neuropathy?

A
  • Symmetric sensory dysfunction
  • distal sensory loss
  • paresthesias
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21
Q

How do you test for diabetic peripheral neuropathy?

A
  • Place a monofilament at a right angle to the plantar surface of the skin of the foot.
  • Increase the pressure until the monofilament buckles.
  • Ask the patient whether or not he/she felt the pressure from the filament.
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22
Q

How should diabetics care for their feet?

A
  • Inspect feet daily for skin cracks and signs of infection between the toes
  • avoid walking barefoot
  • ensure shoes fit appropriately.
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23
Q

What should you look for when examining the feet of diabetics?

A
  • Skin breaks
  • early ulcers
  • decreased pedal pulses
  • delayed capillary refill
  • bony deformities
24
Q

Describe manifestations of autonomic neuropathy

A
  • Gastroparesis
  • orthostatic hypotension
  • impotence
  • neurogenic bladder
25
Q

What interventions did the UK Prospective Diabetes Study compare?

A

Four thousand type II diabetics were assigned to either intensive therapy (sulfonylurea, metformin, and/or insulin) or diet alone.

26
Q

What did the UK Prospective Diabetes Study show?

A
  • Intensive therapy caused a 1% fall in HbA1c and was associated with a 35% reduction in microvascular endpoints (though most of the benefit was attributable to a decreased need to use photocoagulation for retinopathy)
  • Metformin (but not sulfonylurea or insulin) decreased mortality independent of blood sugar control
  • Tight BP control in diabetics reduced mortality
27
Q

How is HbA1c formed?

A
  • Glucose irreversibly attaches to hemoglobin at a rate dependent on blood glucose.
28
Q

What does HbA1c indirectly measure?

A
  • The patient’s average glucose level over the preceding 120 days (the life span of RBCs), although it best correlates with average blood glucose over 56-84 days
29
Q

What will falsely elevate HbA1c?

A
  • Any process that decreases RBC turnover (eg, vitamin B 12 , folate, or iron deficiency)
30
Q

What will falsely decrease HbA1c?

A

Any process that decreases RBC turnover (eg, vitamin B 12 , folate, or iron deficiency)

31
Q

How frequently should HbA1c be checked?

A
  • Every 3-4 months until at goal, then every 6 months
32
Q

What is the goal for HbA1c?

A

HbA1c <7% (an average blood glucose of 154 mg/dL)

33
Q

What is the treatment for type I DM?

A
  • Insulin replacement
34
Q

What are the treatments for type II DM?

A
  • Weight loss
    • exercise
    • Diet
  • oral hypoglycemic medications
  • exogenous insulin
35
Q

Defination of a metabolic syndrome

A

Any three of the following:

  1. Abdominal obesity (waist circumference in men >40 in, women >35 in)
  2. Serum triglycerides ≥150 mg/dL or drug treatment for elevated triglycerides
  3. Serum high-density lipoprotein (HDL) cholesterol <40 mg/dL in men and <50 mg/dL in women or drug treatment for low HDL
  4. BP ≥130/85 mm Hg or drug treatment for elevated BP
  5. Fasting plasma glucose (FPG) ≥100 mg/dL or drug treatment for elevated blood glucose
36
Q

What are the clinical implications of having the metabolic syndrome?

A

Increased risk of developing diabetes and cardiovascular disease

37
Q

What is the body mass index (BMI) measurement?

A

An indirect approximation of body fat

38
Q

How is BMI calculated?

A
  • ([Weight in lbs.]/[height in in.] 2 ) × 703 or
  • (Weight in kgs.)/(height in m.) 2
39
Q

Which BMI level represents being overweight?

A

Between 25 and 29.9

40
Q

Which BMI level represents being obese?

A

≥30

41
Q

In what situation does BMI overestimate body fat?

A

A person with a higher than average percentage of muscle mass

42
Q

Which diseases of the exocrine pancreas can cause diabetes?

A
  • Cystic fibrosis
  • hemochromatosis
  • chronic pancreatitis
43
Q

Which endocrinopathies can cause diabetes?

A
  • Any increase in hormones that inhibit insulin:
    • Cushing (cortisol)
    • glucagonoma (glucagon)
    • pheochromocytoma (epinephrine)
    • acromegaly (growth hormone)
44
Q

What is diabetic ketoacidosis (DKA)?

A
  • A medical emergency where insulin deficiency leads to hyperglycemia, electrolyte disturbances, ketonemia, and metabolic acidosis
45
Q

How does the insulin deficiency precipitate DKA?

A
  • In insulin deficiency, the liver breaks down lipids into ketone bodies resulting in a decrease in blood pH (serum ketones + acidosis).
46
Q

What can precipitate DKA? .

A
  • I’s: I nfection,
  • I nfarction (cardiac, cerebral, mesenteric),
  • I nsulin (prescription dose is too low, patient is noncompliant),
  • I ntraabdominal process (pancreatitis),
  • I ntoxication (alcohol),
  • I diopathic. Also consider physical stress and drugs (eg, glucocorticoids, second-generation antipsychotics)
47
Q

How do you categorize the acid-base abnormality in DKA?

A

Anion gap metabolic acidosis with compensatory respiratory alkalosis

48
Q

What is Kussmaul breathing?

A

Rapid, deep breathing to help increase CO 2 excretion and correct the underlying acidosis in DKA

49
Q

A patient with DKA can have what odor to their breath?

A
  • Fruity, acetone odor
50
Q

What is the treatment of DKA?

A
  • Aggressive IV fluids
  • IV insulin
  • acid-base and electrolyte management (potassium, phosphorus)
51
Q

When can you transition the patient from IV insulin to subcutaneous insulin?

A
  • When the anion gap has resolved and the bicarbonate level approaches normal
52
Q

What are the diagnostic criteria for hyperosmolar hyperglycemia state (HHS)?

A
  • Plasma glucose >600 mg/dL
  • arterial pH >7.3
  • serum bicarbonate >18 mEq/L
  • effective serum osmolality >320 mOsm/kg
  • minimal ketones in serum and urine
53
Q

How do you manage HHS?

A
  • Aggressive IV fluids
  • IV insulin
  • correction of electrolyte abnormalities (such as potassium depletion)
  • monitoring of urine output and mental status
54
Q

What percentage of patients with HHS also present with neurologic abnormalities such as coma?

A
  • 25%-50%.
  • Neurologic changes occur in patients with effective plasma osmolalities above 320 mOsm/kg.
55
Q
A

General Medicine & Family Medicine (150 decks)

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